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Lecture 22

BIO220H1 Lecture Notes - Lecture 22: Antagonistic Pleiotropy Hypothesis, Seabird, Mortality Rate


Department
Biology
Course Code
BIO220H1
Professor
John Stinchcombe
Lecture
22

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Lecture 22: Aging
Important messages
Antibiotics save lives
Overuse of antibiotics is a major problem BUT there are large scale issues that need to be dealt with
Overuse in agriculture; inappropriate prescribing practices, which are being dealt with at a policy/protocol level
In the meantime, folks (including evolutionary biologists) are working on what to do about drug resistant bugs,
and how to extend the useful lifespan of current drugs but you should listen to your doctor
Humans and Fulmars George Fulmar
1950 Birth #64 1992 sees fulmar again (the bird has not aged that much variation in rates of aging)
World’s oldest-known seabird lays an egg at age 66 in Pacific refuge (Wisdom’s 41st egg!) Chanlar Robins
Hydra VS Mayfly
Mayfly lives as adult for 1 day (mating and laying eggs and then dies)
Hydra ~1400 years huge amount of variation between animals
But why has aging evolved? Why do we age at all?
Aging
Aging - proximate and ultimate causes
Costs of reproduction
The evolutionary theories of aging
- Mutation accumulation
- Antagonistic pleiotropy
What is aging or senescence?
Progressive decline in somatic function reflected in reductions in fertility as well as survivorship
Proximate cause progressive degeneration of the soma
Manifestations of aging
General degeneration of the soma
- Impaired function (speed, strength, sight, muscle mass, etc)
- Increased disease (chronic, cancer, organ failure)
Mortality rate increases with age increased age-specific mortality rate
Senescence: an evolutionary mystery
Observation we have evolved to age and die
- Is there an explanation? Appears to be non-adaptive in the extreme
One proximate theory of aging
Oxidative metabolism produces highly reactive free radicals that damage macromolecules (DNA, protein, lipids)
in our bodies
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Vitamins E and C can act as antitoxidants mopping up free radicals
But, this theory also raises some questions
- We have our own defenses and repair mechanisms (e.g. various amino acids act as antioxidants) so why not
ENOUGH repair? Why arent we doing more mopping of free radicals? = CONSTRAINTS!
Life without constraints (alternative of constraints)
Darwinian Demon?
- Ideal organism would maximize all fitness components simultaneously
Begin reproducing at birth, Reproduce at an infinite rate, Live forever
But we have not found one yet so,
- Biological systems are constrained
- Constraints often take the form of trade-offs
Trade-offs affect the evolution of all traits
Display size (morphological trait)
Foraging rate (behavioral trait)
Longevity how long you live (life history trait)
Trade-offs may govern the evolution of DNA repair mechanisms?
DNA repair + longevity (help us live longer)
DNA repair fecundity (spending energy on this, less energy to reproduction and fecundity)
Costs of reproduction?
If yes, then high reproductive rates will accelerate senescence and thereby shorten life span
Reproductive effort
- (+) reproductive rate but () longevity (why don’t we live forever? We are reproducing!)
Reproductive costs in waterstriders
Prediction females induced to reproduce at high rate will have reduced longevity
Test: female waterstriders
Suck guts out of insects trapped on surface energy to making eggs
Hypothesis high reproductive rates accelerate senescence and thereby shorten life span
Design manipulated reproductive rate of females by changing food abundance
Data reproductive rate (# of eggs usually 6-10), longevity, quality of eggs
Longevity
Lives shorer when given lot of food and produce about twice the many eggs
Senescence of the mother can be seen in age-related declines in egg quality
- Normal development
- Developmentally arrested
- Abnormal development
Those reproducing faster and senescing faster, they should produce abnormal eggs earlier
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